A rat model is being developed to investigate the potential mechanisms by which maternal exposure to chemicals during pregnancy alters fetal respiratory tract development, and postnatal function of the respiratory tract. Preliminary data suggest that in utero exposure to cadmium chloride (CdC12) may inhibit surfactant production in the fetal lung possibly by interfering with glycogen utilization. Studies are planned to investigate further the mechanism of surfactant inhibition, by measurement of lung changes in glycogen, and expression of surfactant apoprotein mRNA in fetal and neonatal lungs. An ELISA assay for surfactant protein A (SP-A) is being developed to quantify surfactant levels in fetal lung. To determine if irreversible effects are caused by in utero exposure, neonates at various ages will be evaluated for abnormalities in histological and biochemical indices of pulmonary development, and abnormal changes in pulmonary function in response to chemical challenge. Studies with CdC12 will be repeated using inhalation exposure of dams to mercury vapor. There is some indication that in utero mercury exposure may affect pulmonary development.